The heart increases in mass when subjected to a sustained elevation of systemic arterial blood pressure. Initially cardiac performance is maintained, but as hypertrophic growth continues, cardiac decomposition eventually ensues. The spontaneously hypertensive rat is an animal model of essential hypertension which demonstrates both a compensated and a depressed phase of ventricular performance. To determine the effects of progressive hypertrophy on the ability of the heart to eject blood, the peak stroke and cardiac indices attained during a preload stress will serve to assess to peak pumping ability of normotensive and hypertensive rats over a wide range of ages. The contribution of ventricular filling to stroke output will be evaluated by determining the passive diastolic pressure-volume relations of the left ventricle. Both chamber and muscle stiffnesses which are affected by changes in wall thickness and fibrosis, respectively, will be analyzed. Functional changes also will be related to the morphologic alterations which occur during a chronic pressure overload. The effects of chronic antihypertensive therapy instituted at various stages of hypertrophic growth will determine at what point the hemodynamic and morphologic consequences of hypertension may be altered or reversed. Thus, the overall objective of these studies is to assess the performance, compliance and geometry of the left ventricle during the natural development of hypertrophy in response to a sustained elevation of systemic arterial pressure and to determine the effects of antihypertensive treatment in altering or reversing this disease process.